Socioeconomic Disparities in Community Mobility Reduction and COVID-19 Growth.

OBJECTIVE: To examine differences in community mobility reduction and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outcomes across counties with differing levels of socioeconomic disadvantage. METHODS: The sample included counties in the United States with at least one SARS-CoV-2 case between April 1 and May 15, 2020. Outcomes were growth in SARS-CoV-2 cases, SARS-CoV-2-related deaths, and mobility reduction across three settings: retail/recreation, grocery/pharmacy, and workplace. The main explanatory variable was the social deprivation index (SDI), a composite socioeconomic disadvantage measure. RESULTS: Adjusted differences in outcomes between low-, medium-, and high-SDI counties (defined by tertile) were calculated using linear regression with state-fixed effects. Workplace mobility reduction was 1.75 (95% CI, -2.36 to -1.14; P<.001) and 3.48 percentage points (95% CI, -4.21 to -2.75; P<.001) lower for medium- and high-SDI counties relative to low-SDI counties, respectively. Mobility reductions in the other settings were also significantly lower for higher-SDI counties. In analyses adjusted for SARS-CoV-2 prevalence on April 1, medium- and high-SDI counties had 1.39 (95% CI, 0.85 to 1.93; P<.001) and 2.56 (95% CI, 1.77 to 3.34; P<.001) more SARS-CoV-2 cases/1000 population on May 15 compared with low-SDI counties, respectively. Deaths per capita were also significantly higher for higher-SDI counties. CONCLUSION: Counties with higher social deprivation scores experienced greater growth in SARS-CoV-2 cases and deaths, but reduced mobility at lower rates. These findings are consistent with evidence demonstrating that economically disadvantaged communities have been disproportionately impacted by the coronavirus disease 2019 pandemic. Efforts to socially distance may be more burdensome for these communities, potentially exacerbating disparities in SARS-CoV-2-related outcomes.

Androgen sensitivity gateway to COVID-19 disease severity.

In this communication, we present arguments for androgen sensitivity as a likely determinant of COVID-19 disease severity. The androgen sensitivity model explains why males are more likely to develop severe symptoms while children are ostensibly resistant to infection. Further, the model explains the difference in COVID-19 mortality rates among different ethnicities. Androgen sensitivity is determined by genetic variants of the androgen receptor. The androgen receptor regulates transcription of the transmembrane protease, serine 2 (TMPRSS2), which is required for SARS-CoV-2 infectivity. TMPRSS2 primes the Spike protein of the virus, which has two consequences: diminishing viral recognition by neutralizing antibodies and activating SARS-CoV-2 for virus-cell fusion. Genetic variants that have been associated with androgenetic alopecia, prostate cancer, benign prostatic hyperplasia and polycystic ovary syndrome could be associated with host susceptibility. In addition to theoretical epidemiological and molecular mechanisms, there are reports of high rates of androgenetic alopecia of from hospitalized COVID-19 patients due to severe symptoms. Androgen sensitivity is a likely determinant of COVID-19 disease severity. We believe that the evidence presented in this communication warrants the initiation of trials using anti-androgen agents.